2019年1月11日 星期五

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2009年1月26日 星期一

septic shock



Glucocorticoid therapy may be beneficial to patients who have severe septic shock (defined as a systolic blood pressure <90 mmHg for more than one hour despite adequate fluid resuscitation plus vasopressor administration).
There are no high or moderate quality data to suggest that glucocorticoid therapy is beneficial to patients with less severe septic shock. (See "Clinical evidence" above).
Classification of adrenal reserve as adequate or inadequate fails to identify patients who are more likely to benefit from glucocorticoid therapy. (See "Clinical evidence" above).


We typically administer 50 mg of hydrocortisone every six hours or 100 mg of hydrocortisone every eight hours.


2009年1月25日 星期日

ideal body weight nutrition

men: Ideal Body Weight (in kilograms) = 50 + 2.3 kg per inch(2.54cm) over 5 feet(152.4cm).
women: Ideal Body Weight (in kilograms) = 45.5 + 2.3 kg per inch over 5 feet.

BMI=22 (both sex)
Calorie need=IBW*30Kcal/kg/day
Protein need=Patient current body weight*72.6g/day

2009年1月22日 星期四

acid base

HCO3 PCO2 同向:metabolic,反向:respiratory(氣體對流)

代償之delta=系數*primary之delta

metabolic:
0.25*5 acidosis
0.25*3

respiratory
0104 acidosis
0204 alkalosis(hyperventilation)

2009年1月21日 星期三

IV urine alkalization

sodium bicarbonate 2 vial Q8H, then check urine PH(target>7.2)
If < 7.2, q8 -> Q6, else Q8 -> Q12

2009年1月20日 星期二

warm shock

病人可在warm shock時就爛掉(organ failure和lactic acidosis),等BP掉時可能巳ischemic bowel等等而爛到不行了(腸子要切掉 etc.)

Warm shock: 尿減少 → HR↑,dyspnea(for compensate),organ failure(如ischemic bowel而想吐,這時HR不是因想吐不適而快,用beta blocker會將好不容易的代償除掉而死)

Sinus Tachycardia是要趕快找underlying處理掉(如hypovolumia),而不能用heart rate藥

過敏和septic shock早期因周邊血管擴張而warm之shock,
只有cardiogenic shock的HR沒上昇
稱之為shock應該都會有尿減少的問題

2009年1月15日 星期四

pneumonia lung edema

rhonchi: 水中咕嚕咕嚕聲 --> sputum
crackle: 搓頭髮聲 --> lung edema

CVP

8-12mmHg, mmH2O則>17, 有用ventilator既使非Bipap/CPAP,都會增加

不能只從CVP評估fluid,
Intravascular是否水足夠:CVP + Bun/Cre + 尿量(體重)

2009年1月14日 星期三

AF with RVR

老人怕血壓掉太快(尤其中風希望高),且常心較不好而不敢用CCB或BB,故用amiodarone(rhythm + rate control,故須af小於48hr, else clot打出去.af>48hr沒出血問題包hemorrhagic transformation則先打heparin一陣子才rhythm control--amiodarone或cardioversion;CCB,BB & digoxin無rhythm control,只能rate control)
cardioversion必須要有CR在,才能執行!因有變cardiac arrest或把血栓打出去的問題
amiodarone原IV後PO,突然又須IV時,則重跑一次bolus→maintainance,沒過一天max dose就好,若仍HR>180,則滴amiodarone時又外加個digoxin(老人沒EF<40問題但怕BP掉和心不好而不想用CCB,BB時)
embolism如ischemic stroke若急診(本來)有Af,要用個2天coumadin才可try弄回正常心律(無如用電擊,beta blocker或其它),否則會把心房內的血栓打出去

Af要150以上才會有症狀(有害),否則只要有在滴amiodarone就好,不一定要再加藥到100以下

Amiodarone alone failed →
1. Cordarone 1# QD(not TID) + Digoxin 0.25mgIV Q8H * 3 then 0.125mg PO QD
2. Isoptin(40) 1# TID + Digoxin 0.25mgIV Q8H * 3 then 0.125mg PO QD

2009年1月13日 星期二

INSULIN

RI+NPH BID下:
早ri影嚮中午
早nph影嚮下午/晚上

晚nph影嚮早上

巳進CELL的GLUCOSE不會因藥效過而又再SHIFT出來

早上多打之RI多少U要記下來,
改成以後晚上NPH的量

PHARMACODYNAMICS / KINETICS — Note: Rate of absorption, onset, and duration of activity may be affected by site of injection, exercise, presence of lipodystrophy, local blood supply, and/or temperature.
Excretion: Urine

RI:Onset 0.5 hours, Peak: 2.5-5 hours
Duration: 4-12 hours (may increase with dose)
Time to peak, plasma: 0.8-2 hours



NPH:Onset 1-2 hours, Peak: 4-12 hours
Duration: 18-24 hours
Time to peak, plasma: 6-12 hours

each increase not ot exceed 3-5U propotional to original dosage

2009年1月12日 星期一

Septic shock with ARF

Intubation: 平常要靠BiPAP, septic shock到用iatrogenic agent,不管ABG如何都可on endo

先charge volume,沒出來才考慮Lasix, albumin
若U/O>1cc/kg/hr, fluid challenge不必急著考慮albumin, FP(not FFP),光charge volume + Lasix PRN即可

健保albumin之給付:
http://www.nhi.gov.tw/information/bulletin_file/1845_W0960000040-A03.DOC

Relative intravascular hypovolemia is typical and may be severe. As an example, early goal-directed therapy required a mean infusion volume of approximately five liters within the initial six hours of therapy in the trial described above [17]. As a result, rapid, large volume infusions of intravenous fluids are indicated as initial therapy for severe sepsis or septic shock, unless there is coexisting clinical or radiographic evidence of heart failure.
Fluid therapy should be administered in well-defined (eg, 500 mL), rapidly infused boluses [8,9]. Volume status, tissue perfusion, blood pressure, and the presence or absence of pulmonary edema must be assessed before and after each bolus. Intravenous fluid challenges can be repeated until blood pressure is acceptable, tissue perfusion is acceptable, pulmonary edema ensues, or fluid fails to augment perfusion.
Careful monitoring is essential in this approach because patients with sepsis typically develop noncardiogenic pulmonary edema (ie, ALI, ARDS). In patients with ALI or ARDS who are hemodynamically resuscitated, a liberal approach to intravenous fluid administration prolongs the duration of mechanical ventilation, compared to a more restrictive approach that typically requires large doses of furosemide [27]. Thus, while the early, aggressive fluid therapy is appropriate in severe sepsis and septic shock, fluids may be unhelpful or harmful when the circulation is no longer fluid-responsive. (See "Supportive care and oxygenation in acute respiratory distress syndrome", section on Fluid management).

shock後會有利尿期,這時的補多出多並不是身體覺得水夠,而是利尿所致,更要補水以免脫水(注意bun/cre, electrolyte)

2009年1月4日 星期日

gastric ulcer bleeding

free- strocain

cash - Nexium($45,but coffee ground with stroke free for 3 days)/Takepron($40,$80), Pantoloc($311), Ciketin(for old age, young age will cause impotence etc., $2/1# BID)

Plavix只有在aspirin GI bleeding 且primary care自行評估或GI評估不適合胃鏡後才能用

Stroke + Gastric OB only 亦可用Losec

2009年1月2日 星期五

J01398, UTI, suspect pneumonia?

152326, takepron vs nexium pantaloc?

2008年12月29日 星期一

phrase

discharge:
按時依照醫囑服藥.
定期門診追蹤治療.

2008年12月28日 星期日

AEIOU tips

Mental:
AEIOU TIPS
A - alcohol, anoxia
E - epilepsy
I - insulin (diabetes)
O - overdose
U - uremia, underdose

T- trauma
I - infection
P - psychiatric
S - stroke (cardiovascular)

Alcohol
Epilepsy
Insulin
Overdose
Uremia (and other metabolic causes)

Trauma
Infection
Psychiatric
Stroke


Altered Mental Status
"AEIOU TIPS"
Alcohol/drugsEndocrineInsulinOpiatesUremia

Toxins/traumaInfectionsPsych/porhyriaSAH, shock, stroke, seizure, space occupying lesion

DM treatment


Sulfonylureas are time-honored insulin secretagogues (ie, oral hypoglycemic agents) and probably have the greatest efficacy for glycemic lowering of any of the oral agents. The UKPDS confirmed their safety after years of suspicion from the University Group Diabetes Program (UGDP).
Glipizide (Glucotrol, Glucotrol XL)
Second-generation Sulfonylureas. More potent and exhibits fewer drug interactions than first-generation agents. May cause more physiologic insulin release with less risk for hypoglycemia and weight gain than other sulfonylureas.
Considerable debate exists regarding the best initial oral therapy for patients with type 2 diabetes mellitus. Based on the results of the UKPDS and safety record, patients who are obese (120% ideal body weight) should be started on metformin initially, titrated to at least 2000 mg/d administered in divided doses (during or after meals to reduce gastrointestinal side effects). Patients who are markedly symptomatic may be treated with an insulin secretagogue initially to rapidly alleviate symptoms and then perhaps switched to other agents. Patients with near-normal weight may be treated with sulfonylureas or metformin initially. Short-acting insulin secretagogues (eg, repaglinide, nateglinide) can be used in patients unusually predisposed to hypoglycemia.

Failure of initial therapy usually should result in addition of another class of drug rather than substitution (reserve substitution for intolerance to a drug due to adverse effects). Considerable debate exists regarding second agents added to (or used initially in conjunction with) metformin. The time-honored approach is to add an insulin secretagogue (usually titrated to no more than the half-maximal approved dose to reduce risk for hypoglycemia). However, some experts recommend a glitazone because of the positive effects of these drugs on inflammation and the vasculature. If this strategy is used, a moderate dose of glitazone (as opposed to the highest approved dose) should be used. A therapeutic scheme utilized by the author is listed in Image 11.

The author usually only uses glitazones in cases of metformin intolerance or contraindication because of the side effects of weight gain and edema seen not infrequently with glitazones. Exceptions to the practice might include patients with marked insulin resistance of relatively normal weight, such as patients of Asian heritage. If an insulin secretagogue is being taken by the patient prior to adding a second agent, the patient should be warned about the possibility of inducing hypoglycemia when another agent is added. In such cases, the insulin secretagogue, not the newly added agent, should be reduced.



From: http://emedicine.medscape.com/article/117853-treatment
Emedicine: Diabetes Mellitus, Type 2: Treatment & Medication

2008年12月26日 星期五

High P LOW Ca

A potential complication of calcium therapy is that absorption of some of the administered calcium may promote the development of coronary arterial calcification, which is postulated to be associated with coronary atherosclerosis [34,35]. To help decrease this possibility, the working group for the K/DOQI guidelines suggest that the total dose of elemental calcium (including dietary sources) should not exceed 2000 mg/day [21]. In addition, with the recommended upper limit of plasma calcium of 9.5 mg/dL (2.35 mmol/L), the amount of elemental calcium is usually also reduced to no more than 1500 mg/day. Even these doses of calcium result in positive calcium balance in the setting of vitamin D therapy, which may have untoward long-term consequences. (See "Active vitamin D analogs and calcimimetics to control hyperparathyroidism in chronic kidney disease" and see "Vascular calcification in chronic kidney disease").

2008年12月22日 星期一

cva artery

GCS:http://en.wikipedia.org/wiki/Glasgow_Coma_Scale

NE: http://medinfo.ufl.edu/other/opeta/neuro/NE_main.html
http://www.stroke.org.tw/guideline/guideline_index.asp

ml=widht1(cm) * width2(cm) * cut number / 2
mca=butterfly wings lateral, aca=mercedes anterior(supraventricle more), pca=mercedes 2 legs


When blood pressure control is necessary, the use of vasodilators such as nitroprusside or nitroglycerin should be avoided because of their propensity to increase cerebral blood volume and therefore intracranial pressure. Labetalol is preferred.
Nimodipine — The calcium channel blocker nimodipine was initially used in patients with SAH to prevent vasospasm. (See "Prevention of vasospasm" below). However, despite the vasodilatory effects of nimodipine on cerebral vessels, there is no convincing evidence that nimodipine affects the incidence of either angiographic or symptomatic vasospasm.

Nimodipine is marketed as a cerebral selective drug
































































Artery involvedSyndromePathophysiology
Anterior cerebral artery

Motor and/or sensory deficit (foot >> face, arm)




Grasp, sucking reflexes




Abulia, paratonic rigidity, gait apraxia

Embolic > atherothrombotic
Middle cerebral artery

Dominant hemisphere: aphasia, motor
and sensory deficit (face, arm >leg >foot), may be complete
hemiplegia if internal capsule involved, homonymous hemianopia.




Non-dominant hemisphere: neglect, anosognosia, motor and sensory deficit (face, arm > leg>foot), homonymous hemianopia.

Embolic > atherothrombotic
Posterior cerebral arteryHomonymous hemianopia; alexia without agraphia (dominant
hemisphere); visual hallucinations, visual perseverations (calcarine
cortex); sensory loss, choreoathetosis, spontaneous pain (thalamus);
III nerve palsy, paresis of vertical eye movement, motor deficit
(cerebral peduncle, midbrain).
Embolic > atherothrombotic
Penetrating vessels

Pure motor hemiparesis (classic lacunar syndromes)




Pure sensory deficit




Pure sensory-motor deficit




Hemiparesis, homolateral ataxia




Dysarthria/clumsy hand

Small artery (lacunar) infarct
Vertebrobasilar

Cranial nerve palsies




Crossed sensory deficits




Diplopia, dizziness, nausea, vomiting, dysarthria, dysphagia, hiccup




Limp and gait ataxia




Motory deficit




Coma




Bilateral signs suggest basilar artery disease.

Embolic = atherothrombotic
Internal carotid arteryProgressive or stuttering onset of MCA syndrome, occasionally ACA syndrome as well if insufficient collateral flow.Atherothrombotic > embolic

2008年12月8日 星期一

Cancer Pain

Step-Up of analgesics by WHO
First step: Acetaminophen
Second step: NSAID (careful), or Temgesic (sublingual tablet)
Third step: Codeine, Tramal, Durogesic patch (Fentanyl patch)
Fourth step: oral morphine solution
Fifth step: IV morphine. Auxillary medication: anti-depressant, anxielytics

Chills or Fever Management

1. Never use NSAID in thrombocytopenia patients
2. First line: Acetaminophen
3. Second line: Vena, Hydrocortisone (Solucortef)
4. Third line: Morphine or Demerol (血壓低病患不宜)
5. Fever 應視情況給予antipyretics 例如1: Past history of febrile convulsion (child), 2:Cardiac or pulmonary insufficiency patients, 3 Pregnancy patients, 4: High metabolism 會惡化thrombocytopenia ,6. Fever or chills 是cytokine reaction 臨床無法分別tumor fever or infection, (不管是feverpattern or temperature) 排除infection 之後才能當成tumor fever, Myeloid Leukemia 基本上不會tumor fever, 應視為infection 處理, Hodgkin disease, Lymphoma(AILD like, T cell, NKcell) tumor fever 比較常見。